Under 'Mothball warning sounded by experts', yesterday's Sydney Morning Herald (Fairfax, Feb 7, 2011, page 3, print) ran an article by Kelly Burke about naphthalene.
Describing one infant death and two others developing 'kernicterus, a debilitating disorder which [...] leads to profound brain damage in infants with a common gene defect' after exposure to naphthalene, the article makes terrifyingly clear the possible link between genetic mutations and environmental toxin sensitivity.
Indeed after reading the experts' view on naphthalene being so toxic it should be banned, it becomes clear that 'gene defect' may not be the right way to describe the mutation involved. As mentioned later in the article, that very same 'defect' is carried by 'as many as one in 20 people of Asian, African, Middle Eastern and Mediterranean descent' and confers protection from malaria.
The paediatricians don't say the 'gene defect' means those at risk of catastrophic brain injury from naphthalene should suck it up. Humanely, in my view, they instead advocate the withdrawal of naphthalene. It's tempting to compare this to what's happening (or not) with autism, where even as it's known that something environmental contributes, interest in locating and removing that factor seems nonexistent.
It's funny, isn't it? If your genes, however sturdy they may be in the face of other challenges, are susceptible to a particular toxin, they're labelled 'defective'. Yet toxins such as naphthalene and mercury are still powerfully lethal even in small doses to supposedly 'normal' people. If a toxin is this powerful, it seems to me that the 'defect' isn't in the gene that renders someone extra-susceptible to it, but in the overarching science that fails to ensure product safety across all genetic types.
Of course, banning a product is just one way to go. The other way is to accept that those poor 'defect' carriers (who would be great survivors of malaria) are allowed to die out. But the end point of that chain of decisions would surely be the accumulation of the toxin to a point where other gene-types become noticeably affected too.
Maybe with autism we've already reached that point?